Written by Jesse McLaren, with edits from Meyers
Four patients presented with chest pain or shortness of breath, and ECGs labeled ‘inferior STEMI’. Using principles of hyperacute T waves, do any have inferior occlusion MI?
Patient 1: 60 year old with shortness of breath
Patient 3: 65 year old with chest pain
Patient 4: 55 year old, prior inferior MI, with chest pain
See this recent post on the new and evolving science of hyperacute T waves, including
1. Larger area under the curve relative to QRS
2. Increase symmetry, defined by time from T-wave onset to peak v peak to end.
3. Less concavity associated with hyperacuity
This can help identify false negative STEMI, or STEMI(-)OMI, at risk for delayed reperfusion.
Conversely, T waves are less likely to be hyperacute if they have
1. Small area under the curve relative to QRS size
2. More asymmetry
3. More concavity
This can help identify false positives at risk for unnecessary cath lab activation.
In addition, ischemic STD in aVL is highly sensitive for inferior OMI, and excludes pericarditis. So inferior OMI is highly unlikely in the absence of reciprocal change in aVL. On the other hand, STD in aVL can also be reciprocal to old inferior MI, or less likely from normal variant when STD and TWI are concordant and proportional to negative QRS.
Smith comment: Because the ST vector of normal variant is towards lead II, there usually is NOT ST depression in aVL even though there is ST elevation in III. for both pericarditis and normal variant, the vector results in more STE in II than III, and absence of STD in aVL. Exceptions to this are rare in pericarditis, but not rare in early repol: in normal variant early repol, the ST vector is sometimes vertical (as in patient 3), which does result in STD in aVL. What does all this mean? It means that, if there is STD in aVL, then it is almost certainly not pericarditis (but could be myocarditis). It could be normal variant, but that is not common and you should strongly consider that it is OMI.
Let’s see the outcome of these cases and how the Queen of Hearts performed:
Patient 1: 60 year old with shortness of breath
The T waves in II are tall relative to QRS and symmetric, but it’s the wrong distribution for inferior OMI – with normal lead III and the reciprocal lead aVL. Serial trops were normal.
Queen correctly predicted with high confidence this was NOT an OMI.
Patient 2: 40 year old with chest pain
T waves are tall relative to QRS in III/aVF, but all T waves are asymmetric with a sharp peak. Lead aVL has minimal TWI after isoelectric QRS. Cath lab was activated: normal coronaries, normal troponins.
Queen correctly predicted with highly confidence this was NOT an OMI.
Here's the analysis of the early HATW model, showing how these T waves are NOT hyperacaute despite their size relative to the QRS:
Patient 3: 65 year old with chest pain
T waves area are not large relative to QRS but are symmetric. There is TWI in aVL but this is concordant to its QRS. Anterior leads also have proportional, asymmetric and concave T waves. Cath lab was activated, with mild coronary artery disease and serial troponins were normal.
Queen did not detect any STEMI/STEMI equivalent, and had low confidence this was OMI.
Patient 4: 55 year old, prior inferior MI, with chest pain
Old inferior MI can leave residual inferior STE with resulting STD in aVL, making it difficult to differentiate. But here T waves are shallow and asymmetric. Based on history of old MI, an old ECG was found which was the same, and serial troponins were normal.
Queen predicted with high confidence this was NOT an OMI.
Take home
1. Hyperacute T waves are tall relative to QRS with large area under the curve, symmetry and loss of concavity – and can help identify STEMI(-)OMI at risk for delayed reperfusion
2. Conversely, T waves tall relative to
QRS are less likely to be hyperacute if they have small area under the curve,
asymmetry and more concavity - and can help identify false positive STEMI at risk for unnecessary cath lab activation
3. Reciprocal change in aVL is highly sensitive to inferior OMI (new or old) and excludes pericarditis, and less commonly STD and TWI may be from normal variant when concordant and proportional to negative QRS
MY Comment, by KEN GRAUER, MD (12/1/2024):
- For clarity in Figure-1 — I've reproduced and labeled these 4 tracings.
- Although there is ST elevation in leads I and II — ST elevation is lacking in lead III, and is minimal in lead aVF. As per Dr. McLaren — this distribution is wrong for this to be an inferior OMI.
- But what immediately reduced my suspicion of an acute event — was the diffuse distribution of similar-looking, upright T waves with concave upright (ie, "smiley"-configuration) ST segments.
- To Emphasize: A "smiley" configuration in no way guarantees that ST elevation is benign. That said — an acute OMI is less likely to manifest this appearance, especially when there is prominent J-point notching (as is seen here in leads V3,V4,V5,V6).
- I found the rSR' configuration seen in all 3 inferior leads to be curious — though of uncertain (if any) significance.
- 2 additional features that immediately dissuaded me from considering acute inferior OMI were: i) That in lead aVL — the ST segment is not depressed and the T wave is upright; — and, ii) That the normal gently upsloping, slight amount of J-point ST elevation is present in leads V2 and V3 — whereas this feature is lacking when posterior OMI (that so often accompanies inferior OMI) is present.
- Bottom Line: Taken together — the combination of the above findings allowed me to quickly conclude that inferior OMI was unlikely.
- As per Dr. McLaren — the inferior T waves are asymmetric with a narrow peak, which is clearly uncharacteristic of hyperacute T waves. That said — a significant amount of ST elevation is present in all 3 of the inferior leads.
- I put a BLUE question mark over the T wave inversion in lead aVL — because while the depth of this T wave inversion is shallow — I thought the width of the T wave base was wider-than-expected given the tiny size of the QRS complex in this lead. I was concerned that the ST-T wave in lead aVL might represent a reciprocal change.
- My concern was reduced on assessing ST-T wave appearance in the chest leads — because all 6 chest leads showed a certain amount of J-point ST elevation, with a gently upsloping ST segment culminating in an upright T wave. The overall ST-T wave appearance in leads V2-thru-V5 was very similar to that seen in the inferior leads (ie, There is essentially no localization of the ST elevation that is seen — which in itself is another finding against acute OMI).
- J-point notching is seen in leads V4,V5,V6 (and it might also have been seen if there was not so much artifact in lead V3). Similar notching is also seen in the inferior leads.
- As was the case for ECG #1 — the normal-appearing ST-T wave appearance in leads V2 and V3 in ECG #2 essentially rules out posterior OMI. So, while lack of posterior OMI does not exclude the possibility of acute inferior OMI — it does make this much less likely.
- Bottom Line: Taken together — the combination of the above findings allowed me to quickly conclude that inferior OMI was unlikely. Assuming specifics of the chest pain history did not suggest pericarditis — I suspected the generalized ST elevation in ECG #2 most likely represents a repolarization variant.
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| Figure-1: I've reproduced and labeled the 4 ECGs in today's case. |
- I thought this tracing had similarities to ECG #1 and ECG #2 that favor no OMI, These include: i) ST elevation manifests a distinct upward concavity ("smiley"-configuration) — and is generalized rather than localized; — and, ii) The upward sloping J-point ST elevation in leads V2 and V3 essentially rules out posterior OMI.
- I put a BLUE question mark over the T wave inversion in lead aVL because I could not rule out the possibility that this might represent an acute reciprocal change. That said — given that the QRS in lead aVL is predominantly negative, I thought the relative size of the inverted T wave is not disproportionate to QRS size in this lead. I suspect this T wave inversion in lead aVL is normal and not an acute reciprocal change.
- QRS amplitude is not reduced in any leads (as it may sometimes be with acute infarction).
- The QTc is relatively short (whereas the QTc is more likely to be longer with acute OMI).
- Bottom Line: The combination of the above findings led me to suspect that inferior OMI was unlikely. The main concern I had — was that the relative amount of J-point ST elevation in lead V3 is more than is usually seen with repolarization variants. Finding a prior ECG on this 65yo patient could prove invaluable for excluding an acute event.
- As a single tracing (ie, before I learned that ECG #4 was unchanged from a previous ECG) — I had no idea if the inferior lead Q waves with subtle-but-real ST elevation with a hint of terminal T wave inversion was new or old (ergo the BLUE question marks I added to each of the inferior leads).
- Similarly — I had no idea if the subtle, mirror-image opposite ST-T wave depression in lead aVL might (or might not) represent an acute reciprocal change (ergo the RED question mark I placed in lead aVL). For me then — it was not the appearance of the ST-T waves in leads II,III,aVF and aVL that ruled out acute (or recent) inferior OMI — but rather finding a prior ECG that showed no new changes.
- Given that this 55yo presented with new CP — I was definitely concerned by the slight amount of ST elevation in association with ST segment straightening in leads V2,V3,V4 (as per the RED lines parallel to the ST segments in these leads).
- Bottom Line: Finding a prior ECG on this patient ruled out a new acute inferior OMI. But in this 55yo patient with known coronary disease and new CP — regardless of the negative prediction by QOH — I would not be comfortable negating the possibility of LAD OMI on the sole basis of this single ECG.
